Anti-arrhythmia devices and methods of use

ABSTRACT

An apparatus and method of use are disclosed for treating, preventing and terminating arrhythmias. In particular, the apparatus is implantable within or on various tissues and structures and is used to prevent or block conduction of aberrant impulses. A variety of methods of the present invention may be used to attack arrhythmias by short-circuiting impulses, inducing fibrosis, ablating tissue or inducing inflammation. In addition, the device and methods may also be used to treat aneurysms. The device may also be used to treat hypertension, and to function as a blood pressure regulator.

CROSS REFERENCE TO RELATED APPLICATIONS

[0001] The present application claims priority to U.S. ProvisionalPatent Application No. 60/303,573, filed Jul. 6, 2001, whose contentsare fully incorporated herein by reference.

BACKGROUND OF THE INVENTION

[0002] Cardiac arrhythmia affects millions of people worldwide and isbroadly defined as an abnormal or irregular heartbeat that may involvechanges in heart rhythm, producing an uneven heartbeat, or heart rates,causing a very slow or very fast heartbeat. Common types of arrhythmias,explained in further detail below, include bradyarrhythmias andtachyarrhythmias, both being typically ventricular or supraventricularin origin.

[0003] Bradyarrhythmias are slow heart rhythms (e.g., less than 60 beatsper minute) that may result from a diseased or failing sinoatrial (SA)node, atrioventricular (AV) node, HIS-Purkinje, or bundle branch system,as explained in further detail below. Ventricular arrhythmias arearrhythmias that begin in the lower chambers of the heart. In contrast,supraventricular arrhythmias are arrhythmias that originate above theventricles of the heart, such as the upper chambers (i.e., atria) or themiddle region (e.g., AV node or the beginning of the HIS-Purkinjesystem). Ventricular and supraventricular arrhythmias are generallycharacterized by accelerated rates (e.g., more than 100 beats perminute) that exceed what is considered normal heartbeat rhythms (e.g.,between 60 and 100 beats per minute).

[0004] The most common type of supraventricular arrhythmia is atrialfibrillation, with incidence of more than a quarter-million cases eachyear in the U.S. alone, and a prevalence of nearly 2.0 per 1000 USpatient-years. To better understand the mechanism and characteristics ofatrial fibrillation, a general understanding of the mechanical andelectrical activity of the heart is helpful. For this purpose, attentionis directed to FIG. 1.

[0005]FIG. 1 depicts a cross-sectional diagram of a normal, healthyheart 10. The heart 10 is a four-chamber, double-sided pump made ofmuscle tissue that contracts when subjected to electrical stimulation.The electrical stimulation that produces a heartbeat originates in theSA node 12, located at the junction of the superior vena cava 14 withthe right atrium 16, and spreads radially through the atria causing themuscle of the heart's upper chambers to contract and pump blood to theventricles. From the atria, the electrical signal then converges on theAV node 18, located in the right posterior portion of the interatrialseptum. The impulse from the AV node 18 then passes to the bundle of HIS20, which branches at the top of the interventricular septum 22 and runssubendocardially down either side of the septum, and travels through thebundle branches 24. The signal then passes to the Purkinje system 26 andfinally to the ventricular muscle causing the lower chambers of theheart to contract and pump blood to the lungs and the rest of the body.After contraction of the lower chambers, the sinus node initiates thenext rhythm or heart beat and the entire cycle is repeated. In general,it is rate of discharge from the SA node 12 (also referred to as thenormal cardiac pacemaker) that determines the rate at which the heart 10beats.

[0006] This synchrony of contraction between the atria and ventriclesproduces a normal heartbeat. In its broadest sense, atrial fibrillation(AF) represents a loss of synchrony whereby the atria quiver (beating ata rate of about 600 beats per minute) instead of beating or contractingeffectively. The loss of atrial contraction and conduction of electricalsignals from the atria to the ventricles often cause blood to pool andclot in the atria, and especially in the atrial appendages. If the clotbecomes dislodged from the atrium, it can travel through the bloodstreamand create a blockage in a vessel that supplies blood to the brain,resulting in stroke. It is estimated that fifteen percent of all strokesoccur in people with AF, which translates to about 90,000 strokes eachyear in the United States alone.

[0007] Conventional therapy or treatment options for AF includemedication, AF suppression and surgery. Medication or drug therapy isgenerally the first treatment option employed to control the rate atwhich the upper and lower chambers of the heart beat. Conventionalmedications used to treat AF include beta-blockers, such as metoprololor propanolol, and calcium-channel blockers, such as verapamil ordiltiazem, which depress conduction and prolong refractoriness in the AVnode. Other medications such as amiodarone, ibutilide, dofetilide,propafenone, flecainide, procainamide, quinidine and sotalol are used toaffect the electrophysiology of the heart to maintain normal sinusrhythm and can thereby terminate or, in some cases, prevent AF. Althoughanticoagulants or blood-thinners such as warfarin or aspirin are notdesigned to treat AF, these medications are often used to reduce therisk of clot formation and stroke which, as previously discussed, oftenoccur in patient's suffering from AF.

[0008] AF suppression, frequently a second treatment option for patientswith AF, may be accomplished using an implanted pacemaker to stimulatethe heart in a way that preempts any irregular rhythms. In general, thepacemaker stimulates or overdrives the heart at a rate slightly higherthan its normal, intrinsic rate. Overdriving the heart enables thedevice to control the heart rate and, thereby, suppress potentialepisodes of AF.

[0009] Another alternative treatment for AF is surgery. In general, anelectrophysiology study is first performed to characterize thearrhythmic event. This study usually includes mapping the exactlocations of the electrical impulses and conduction pathways along thecardiac chambers using conventional mapping techniques. After locatingthe cardiac tissue that is causing the arrhythmia, the tissue is thensurgically altered or removed to prevent conduction of aberrantelectrical impulses in the heart. One example of a surgical procedureused to treat cardiac arrhythmias is the Maze procedure.

[0010] The Maze procedure is an open-heart or percutaneous surgicalprocedure designed to interrupt the electrical patterns or conductionpathways responsible for cardiac arrhythmia. Originally developed by Dr.James L. Cox, the Maze procedure involves carefully forming a “maze” ofsurgical incisions (from which the procedure's name is derived) in bothatria to prevent the formation and conduction of errant electricalimpulses, while still preserving the function of the atria. Theincisions channel or direct the electrical impulses along the heart tomaintain synchrony of contraction between the atria and ventricles ofthe heart, thereby producing a normal heartbeat. In addition, resultingscar tissue generated by the incisions also prevents formation andconduction of aberrant electrical signals that cause AF, therebyeradicating the arrhythmia altogether.

[0011] Although surgical intervention, such as the Maze procedure, hasproven successful in treating AF, these procedures are highly invasive,generate many postoperative complications, require lengthy patientrecovery times and are quite costly. As a result, minimally invasiveablation techniques have become more popular and have been offered as analternative treatment to surgical intervention for patients sufferingfrom AF.

[0012] Cardiac ablation techniques typically involve the removal ordestruction of cardiac tissue and the electrical pathways that cause theabnormal heart rhythm. In general, cardiac ablation is less costly, hasfewer side effects and requires less recovery time for the patientcompared to more invasive procedures. There are various methods by whicha cardiac ablation procedure may be performed. These methods and energymodalities include cryoablation, radiofrequency (RF) ablation, laserablation, microwave, vaporization, balloon ablation, drug elution andphotodynamic therapy.

[0013] During an ablation procedure, an electrophysiology study is firstperformed to characterize the arrhythmic event and map the preciselocations that exhibit the arrhythmia. Once these sites are identified,an ablation catheter is maneuvered to each of these sites and asufficient amount of energy is delivered to ablate the tissue. As aresult, the energy destroys the targeted tissue and, thus, makes itincapable of producing or conducting arrhythmia, while leaving theadjacent healthy tissue intact and functional.

[0014] In addition to ablating the specific arrhythmic tissue sites,alternative ablation procedures, such as cardiac segmentationprocedures, have been developed to mechanically isolate or re-directerrant electrical signals in the heart. These procedures typicallyinvolve forming one or more linear or curvilinear lesions in the walltissue of the heart to segment the cardiac chambers, similar to theabove-described Maze procedure. These segmented lesions are generallyformed in the atrial tissue of the heart, although accessory pathways,such as those through the wall of an adjacent region along the coronarysinus, have also been produced.

[0015] Advances in mapping and characterizing cardiac arrhythmias,particularly AF, have provided much insight into the mechanism of AF.Research has shown that there are at least six different locations inthe left and right atria of the heart where relatively large, circularwaves of continuous electrical activity (i.e., macro reentrant circuits)occur in patients suffering from AF. Recently, it has been determinedthat these reentrant circuits or wavelets may actually be confined to alimited area near the pulmonary veins. In other words, some forms of AFmay even be triggered or maintained by a single focus of automaticfiring. As a result, several procedures have been developed whereby oneor more ablation segments or lesions are formed in tissue to isolate thepulmonary veins and thereby block the electrical impulses that cause AF.

[0016] Although catheter based ablation procedures are less invasivethan conventional surgical procedures, there are various complicationsthat may occur. Examples of possible complications include ablationinjuries, bleeding, hematoma, pericardial effusion and cardiactamponade, failure of the procedure, scar formation and stenosis. Inaddition, the time course of lesion maturation and scar formationfollowing cardiac ablation procedures often result in delayed onset ofelectrical isolation and high incidence of post-operative atrialfibrillation.

[0017] In view of the above, there is a need for a minimally invasivedevice and more effective and efficient methods to treat cardiacarrhythmias. In particular, it is desirable that the methods have a highsuccess rate at treating arrhythmias, have minimal to no side-effects orrelated complications, and can be completed more rapidly thanconventional methods. In addition, the treatment methods should alsoreduce patient recovery times and hospital costs. Overall, the method oftreatment should also improve the quality of life for patients.

BRIEF SUMMARY OF THE INVENTION

[0018] In general, the present invention contemplates an implantabledevice and method for modifying conduction, electrical connection andpropagation properties in a tissue and/or treating cardiac arrhythmias.The device comprises a structural platform made of a biocompatiblematerial, wherein the platform may be conformable to a shape of a targettissue site. In addition, the platform may also include a treatmentcomponent sized and shaped to induce a fibrotic response in the targettissue. The treatment component may also be configured to causesufficient fibrotic response so as to substantially eliminate cardiacarrhythmias.

[0019] The present invention also contemplates a method of treatingcardiac arrhythmias. In general, the method comprises delivering atreatment device to a target site and manipulating the device to conforma shape of the device to a shape of the target site. The method may alsoinclude modifying a tissue makeup at the target site and allowing themodification of tissue makeup to proceed so as to induce a response thatresults in electrically decoupling the tissue. The method may furtherinclude leaving the treatment device implanted at the target site.

[0020] Additionally, the present invention contemplates a device formodifying tissue at a target tissue site of an organ, wherein the devicecomprises at least one deployment platform. The deployment platform mayinclude a treatment component configured to induce a material tissueresponse at the target tissue site. In addition, the treatment componentmay also be configured to induce a material tissue response sufficientto modify local physiologic properties of the organ so as to achieve adesired therapeutic goal for the organ.

[0021] The present invention also contemplates a method of inducing amaterial tissue response at a target site, wherein the method includesdelivering a treatment device to the target site and ensuring contact ofa treatment component of the treatment device with tissue at the targetsite. The method may also include inducing the material tissue responseat the target site as a result of ensuring contact of the treatmentcomponent with the tissue and allowing the material tissue response tocontinue at the target site at least until a therapeutic goal issubstantially achieved.

BRIEF DESCRIPTION OF THE DRAWINGS

[0022] Other features and advantages of the present invention will beseen as the following description of particular embodiments progressesin conjunction with the drawings, in which:

[0023]FIG. 1 is a cross-sectional diagram of a normal, healthy heart;

[0024]FIG. 2A illustrates another embodiment of the device in accordancewith the present invention;

[0025]FIGS. 2B and 2C are sectional views of other embodiments of animplanted device in accordance with the present invention;

[0026] FIGS. 3A-3C illustrate sectional views of various embodiments ofan implanted device in accordance with the present invention;

[0027]FIG. 4A illustrates the various layers of a vessel;

[0028]FIG. 4B illustrates areas of high sheer at various tissue pointsin accordance with the present invention;

[0029]FIGS. 5A and 5B illustrate other embodiments of the device inaccordance with the present invention;

[0030]FIGS. 6A and 6B are sectional views of various embodiments of animplanted device in accordance with the present invention;

[0031]FIG. 7 is a perspective view of an embodiment of the device inaccordance with the present invention;

[0032] FIGS. 8A-8C illustrate perspective views of other embodiments ofthe device in accordance with the present invention;

[0033]FIGS. 8D and 8E illustrate sectional views of various embodimentsof an implanted device in accordance with the present invention;

[0034]FIGS. 9A and 9B illustrate perspective views of variousembodiments of an implanted device in accordance with the presentinvention;

[0035]FIGS. 10A and 10B illustrate perspective views of variousembodiments of an implanted device in accordance with the presentinvention;

[0036]FIG. 11 illustrates a perspective view of a ring-shaped embodimentof the device in accordance with the present invention;

[0037] FIGS. 12A-12C illustrate sectional views of various embodimentsof an implanted device in accordance with the present invention;

[0038]FIG. 12D illustrates a perspective view of an embodiment of animplanted device in accordance with the present invention;

[0039]FIG. 12E illustrates a section view of an embodiment of a deviceimplanted on an internal surface of a vessel in accordance with thepresent invention;

[0040]FIG. 12F illustrates a perspective view of an embodiment of adevice implanted on an external surface of a vessel in accordance withthe present invention; and

[0041]FIG. 12G illustrates a perspective view of an embodiment of animplanted device in accordance with the present invention.

DETAILED DESCRIPTION OF THE INVENTION

[0042] In one preferred embodiment of the invention, a stent-shapeddevice 30 may be used to treat, prevent and/or terminate arrhythmias. Itshould be noted that use of the term “stent” is not meant to be limitingbut, rather, is used for reader convenience and brevity. In general, thedevice 30 resembles an “inverse sock” fabricated from a fine nettingmaterial (e.g., Nitinol®, spring-tempered stainless steel, cloth fiber,etc.). The netting material may be self-expandable, causing the device30 to tightly conform to the structure into which it is placed. In oneembodiment, a high spatial frequency of fine material (i.e., finefibers, elongate elements (discussed in further detail below) orstrands) is used to fabricate the device 30. This design provides thedevice 30 with added axial conformability and trans-axial capabilities,resulting in improved tissue adhesion and fit.

[0043] The device or deployment platform 30 of the present invention mayalso be characterized by its ability to bend longitudinally andtrans-axially. This capability enables the device 30 to conform to anydesired biologic shape, including, but not limited to, the wall of anartery, vein, cardiac chamber or other biologic target structure. Inaddition, the device 30 may also be characterized by its ability toexpand in a radial direction, and continue to conform to a shape thatmay change. In one embodiment, the device 30 may have a maximum size,beyond which the device 30 does not expand. This configuration preventsthe tissue structure 36, into which the device 30 is placed, fromgrowing or expanding above a predetermined size.

[0044] As shown in FIG. 2A, one or more hollow protrusions 34 (discussedin further detail below) lie on an external surface of the device 30.Upon radial expansion of the device 30, via self-expansion, balloonexpansion, or other means, the protrusions 34 pierce or embed into thetissue 36 target site of the lumen, as illustrated in FIG. 2B. Theprotrusions may penetrate the vessel wall either partially or completely(as shown in FIGS. 2B and 2C), gaining access to any cells at anylocation in or on the structure. The protrusions may also be solidrather than hollow, as may be desirable if drug delivery is notcontemplated. In addition to anchoring the device 30, the protrusionsalso serve various other functions as described in further detail below.

[0045] In one embodiment, injection from a drug delivery balloon (notshown) causes the hollow protrusions 34 to conduct the drug to theadventitial surface of the lumen or vessel. The drug may then cause celldeath, fibrosis or inflammation, all of which may be used to combatarrhythmia depending on the type of drug used and desired tissueresponse.

[0046] As disclosed in further detail below, the device 30 of thepresent invention and its methods of use are designed to achieve avariety of therapeutic goals including, but not limited to, prevention,treatment and/or elimination of arrhythmias. Studies have shown thatsome forms of AF originate in the pulmonary veins 44 or coronary sinus.More specifically, it has been determined that sources of AF originatein atrial tissue that is on the surface or ingrown into the vessel as itenters the left atrium (i.e., at or near the ostium of the vesselentrance into the atrium). Although further references will be madespecific to the pulmonary veins 44, it is understood that other vessels(e.g., coronary sinus, aorta, abdominal aorta, pulmonary artery, atrium,cerebral vessels, etc.) are also included within the scope of thepresent invention.

[0047] When positioned at this target site, the device 30, preferably inan expanded state, eliminates or neutralizes the electrical activity andconductivity of the atrial cells on the pulmonary vein so that AFstimulation is either prevented (by ablating the atrial cells) or theimpulses are prevented from propagating into the atrium. In principle,it is distortion of the anatomy, such as the ostium, by a luminal orextra-luminal device 30 that permits sclerosis, cell death, scarformation, mechanical injury, laceration or any combination of theseresults to attack impulse stimulation and conduction. The following arebut a few examples of atrial tissue ablation methods. It is understoodthat other tissue modification and ablation methods though notspecifically disclosed herein are also included within the scope of theclaimed invention.

[0048] In one embodiment, the device 30 (with or without graspingmembers, as discussed in further detail below) is radially expanded, forexample via self-expansion and/or balloon expansion, in the lumen oroutside the lumen (e.g., on the adventitia) of the pulmonary vein 44.Alternatively, the device 30 may be expanded on an endocardial 40 orepicardial 42 surface of the heart. Expanding the device 30 sufficientlybeyond the normal diameter of the pulmonary vein 44 causes the vessel toseverely stretch, which induces cellular changes that alter the biologicbehavior of the tissue 36.

[0049] In particular, the fine network of blood vessels called the “vasavasorum,” which are located on the outer surface of many blood vesselsand supply the vessel wall itself with blood, are subsequentlycompressed by this over-stretching, resulting in fibrosis. This vesselover-stretch may further produce tissue/vessel ischemia and othertension effects that may also induce fibrosis. The fibrosis may beinduced by many mechanisms including, but not limited to, growth factors(Hypoxia Inducible Factor-1 alpha (HIF-1alpha), Vascular EndothelialGrowth Factor (VEGF), etc.) and cytokines.

[0050] Lack of blood to the atrial cells combined together with thefibrosis induced by the over-stretching renders the atrial cellsinactive. However, any unaffected cells upstream from the over-stretchedarea can still produce the stimulatory potentials. While these cells maystill produce a stimulus, it cannot be propagated through the fibroticarea in and/or on the vein due to the fibrosis electrically decouplingthe affected cells.

[0051] Vessel over-stretch, or other mechanical tissue change, isaccomplished initially by deployment of the device 30. However,continued or chronic over-stretch may be achieved by simply maintainingthe oversized device 30 within the vessel. As such, the over-stretchitself may also be enough to induce adventitial and/or medial fibrosissimply due to the stretch process.

[0052] The purpose of the fibrosis induced by the device 30 may beseveral-fold. In one embodiment, the fibrosis may serve to mechanicallyprevent organ or gross body expansion. For example, the structuralcomponent of the device 30 may be tailored to expand only to a certaindegree. Fibrosis formed in the tissue 36 functions to tightly attach or“glue” the device 30 to the tissue. Moreover, the fibrosis serves toanchor the tissue of interest to the supporting structure/device 30, andeven integrate the device completely into the tissue. As such, furtherexpansion of the biological structure is prevented due to the mechanicalproperties of the device 30 and due to the fibrosis itself (which maydevelop and grow to contain collagen that will further inhibitmechanical expansion).

[0053] Alternatively, the fibrotic response from the expandable device30 may enable the tissue 36 to retain sufficient pliability to maintainnormal tissue (or body organ) function, yet increase its overallstructural strength. For example, fibrosis may be induced to strengthenthe wall of a cardiac ventricle when the device 30 is placed on theinside of the chamber/structure, while still allowing the ventricle tocontract, move and fulfill its normal function. However, the fibrosisalso prevents ventricular expansion beyond a certain predetermined size.In general, the material make-up of this type of pliable fibrous tissuecomprises more elastin and other pliable materials than collagen.

[0054] Alternatively, the fibrotic response may be stimulated to asevere degree causing a process of negative remodeling or contraction.This response, well known by those skilled in the art, results innatural scar formation that promotes wound contraction or shrinkage. Theamount of fibrosis contraction may be controllable, via devicematerials, structure and other components, and may range from noremodeling to a small/medium/large amount of negative remodeling(resulting in contraction). This would be of particular use inpreventing expansion of an aneurysm, as in the abdominal aorta or thecerebral vessels. The degree of remodeling is based upon thepre-selected application and desired response.

[0055] In addition to device expansion, device materials and structuremay also be used to biologically guide the cellular and biologicfeatures of the eventual tissue response and/or therapeutic goal. Forexample, the device 30 may be configured to induce elastance in thetissue or an elastin-rich fibrosis (e.g., stimulate elastin synthesisand cellular growth) that is quite flexible and visco-elastic.Alternatively, the device may be configured to stimulate growth ofdensely packed collagen that may mimic the need for such bioabsorbabletissue 36. In the case of collagen, the induced tissue 36 is quiteinelastic and, thus, prevents tissue and device expansion. As such,inducing a simultaneous combination of elastin and collagen may simulateany range of mechanical properties for both tissue 36 and device 30.

[0056] In an alternate embodiment, the device 30 may be configured tocontrol the biologic features of the fibrosis and its cellularity. Forexample, a highly cellular scar may be formed or, alternatively, lesscellular tissue may be produced due to device structure and/ormaterials. In another embodiment of the invention, the device 30 may becoated with a material to stimulate less collagen or elastin growth andincreased glycose-aminoglycan and other components of extra cellularmatrix production.

[0057] There are numerous additional methods by which to inducefibrosis, thereby preventing aberrant impulse conduction through tissue36. In addition to over-stretch injury, inflammation and toxicity mayalso be used, as discussed further below.

[0058] Inflammation induced fibrosis may be accomplished using anembodiment of the device 30 having prongs or tissue grabbers 34 thatpenetrate partially into or completely through the vessel. A chemicalirritant located on the surface of the prongs 34 causes the desiredinflammation and, thereby, induces fibrosis in the atrial tissue 36. Ingeneral, the fibrosis occurs in and around the three-dimensionalstructure and, thus, it is the structural configuration of the device 30that guides/determines the eventual fibrosis configuration. As discussedin further detail below, the device 30 may be configured in anyarbitrary shape, size and density and may include one or more of avariety of chemicals/agents/substances. Alternatively, the device 30 maybe placed only against the interior surface and tissue ablation maystill occur on the outer surface of the biologic structure.

[0059] In an alternate embodiment, only the tips of the prongs 34 arecoated with a chemical irritant, the remainder of the stalk of eachprong 34 being uncoated and, thus, inactive. Further, the interior ofthe prongs 34 may house additional chemical irritant that elutes outinto the outer regions of the vein, thereby gradually inducing afibrotic response that prevents initiation or propagation of thearrhythmia. Examples of such chemical irritants include, but are notlimited to, metallic copper, zinc, talc, polymers, drug-elutingpolymers, tetracycline or other fibrosis-inducing substances.

[0060] In another embodiment of the invention, a toxic substance mayalso be used to induce fibrosis. The substance is released into thetissue 36 by the device 30, via a delivery device and/or any of thepreviously disclosed methods, and either kills atrial cells or preventstheir depolarization and/or conduction. Thus, the resulting fibrosis orscarring inhibits cell stimulation and/or impulse propagation and,thereby, prevents or terminates the arrhythmia. Examples of toxicsubstances include, but are not limited to, metallic copper, zinc,polymers, poly-lactic acid, poly-glycolic acid, tetracycline, talc orany other chemicals/agents/substances capable of fibrosis induction.

[0061] Use of a conventional stent-shaped device 30 near the atrialentrance of the pulmonary vein 44, or entrance of any other vessel,generally distorts the ostium-atrial entrance geometry in a radial(i.e., outward, trans-axial) direction. As previously discussed, thisconfiguration may be effective in attacking arrhythmias sincecell/tissue death or fibrosis may successfully interrupt theconduction/stimulation of AF. In some instances, there may be cellsextending up and down the ostial wall that may escape the fibroticprocess. In such an instance, a flared device may be used.

[0062] Referring to FIGS. 3A and 3B, an alternate embodiment of thedevice 30 of the present invention includes one or more outwardly flaredportions 46. When positioned within a patient, the flared end 46 islocated at or near the ostium or vein-atrial interface. In addition toanchoring the device 30, this device configuration also draws tissueinto the ostium and, in so doing, causes the cells to cease conduction,either by death or fibrosis. Inevitably, distortion of the ostiumprevents propagation or conduction of impulses into the atrial tissue 36and, thereby, terminates arrhythmias.

[0063] This mechanical distortion of the tissue and/or ostium geometry,in effect, brings the ostium into the lumen of the device 30. In otherwords, cells that were previously within the atrium at the ostial siteare relocated within the new lumen created by the mechanical support ofthe device 30.

[0064] In another embodiment, illustrated in FIG. 3C, the flared end 46of the device 30 may further include a lip or ring 48 that extends outinto the atrium 50. As such, the ring 48 functions to prevent conductionand/or generation of impulses beyond the ostium and, in so doing,terminates AF or prevents its conduction into the atrial tissue.

[0065] In general, the device 30 of the present invention functions tostretch not only the vein, but also the ostium. This stretch causestension in the vessel wall and compression of blood supply in eithercapillary form or vasa vasorum. The resulting compression may furtherproduce tissue ischemia and other tension effects and induce fibrosisand/or collagen/matrix formation to interrupt electrical impulsegeneration and conduction. As disclosed in further detail below, toxicor inflammatory agents may also be included with the device of thepresent invention to prevent, treat and/or terminate arrhythmias.

[0066] Although compression forces alone may induce an inflammatoryresponse, the anatomy of a device-tethered vein in communication with afree atrial wall and the relative motion between the two structures mayalso induce irritability and inflammation. Alternatively, the device 30may also prevent or change this relative motion. However, even in theseinstances, impulse induction and conduction may still be interrupted oreliminated.

[0067] In addition to inducing fibrosis via tissue compression, tissueinjury or chemical/agent inducement, the device 30 of the presentinvention may also be used to stimulate proliferation of cells in theadventitial or outside region of a vein or artery, where electricallyactive cells reside and/or conduction occurs. An illustration of thevarious tissue layers of an artery/vein is shown in FIG. 4. In general,the vessel 52 includes three layers or “tunics.” The tunica intima 54comprises an inner endothelial cell layer 56 (i.e., the endothelium), asubendothelial connective tissue 58 and a layer of elastic tissue 60(i.e., the elastica interna). In contrast, the tunica media 62 comprisessmooth muscle and the tunica adventitia 64 comprises connective tissue.

[0068] Cell proliferation, stimulated by the device 30 and/or methods ofthe present invention, consists of fibrous tissue, fibroblasts,myofibroblasts and other extra-cellular matrix elements that serve toisolate the electrically active cells that cause the arrhythmia. Assuch, cells are not necessarily killed or injured, as with ablationtechniques. Moreover, the proliferation and stimulation of fibrosis(including fibroblasts, fibrocytes, collagen and extra cellular matrixformation) occurs throughout the vessel wall (i.e., a transmuraleffect), including within the intima 54.

[0069] Cell proliferation and other transmural effects occur fromstretch and tension induced in the wall of the artery or vein. Thetension within the vessel wall, assuming the wall is relatively thin, isgoverned by LaPlace's Law: T=P×R (wherein: T=wall tension, P=pressurewithin the structure, and R=radius of the structure).

[0070] As previously disclosed, tension can cause collapse of arterialor venous vasa vasorum, thereby making the vessel ischemic. Also, if thetension is too high, injury or laceration (small to large, depending onthe tension applied) to the vessel may occur. However, it has been shownthat such tension may also actually stimulate proliferation of fibroustissue. Therefore, by controlling the amount of tension or injury (withor without tissue laceration), the degree of fibrosis and proliferationcan also be controlled. Moreover, the tissue proliferation is typicallyproportional to the tension and injury created.

[0071] Unlike conventional ablation technologies which promotewidespread cell death and cause the intima 54 to thicken to the pointwhere vascular stenosis occurs (an additional complication of ablationprocedures), the device 30 of the present invention carefully controlsthe injury and, thus, does not stimulate such stenosis. For example, thetransmural effects of the device 30 and associated methods may affectthe adventitia with fibrosis; however, the inner lumen remainsrelatively unaffected. Moreover, the mechanical and/or structuralsupport offered by the implant 30 further limits or eliminates theproblem of fibrosis restricting the lumen (which generally also inducesstenosis).

[0072] For example, high shear at sharp points (such as those shown byreference numeral 66) can be placed at various points on the tissue 36using the device 30, as shown in FIG. 4A, thus creating localizedfibrosis that extends transmurally from intima 54 to adventitia 64.These focal areas can then be used to create conductionisolation/blocks, due to the non-arrhythmic/non-conductive nature of thefibrous tissue and matrix. Thus, it is the fibrotic tissue that preventsconduction or generation of arrhythmic impulses.

[0073] Alternatively, the device 30 can also be used to induce fibrosisby inflammation induction. It has been determined that subsequenthealing of the inflammation is a long-term cause of fibrosis. Thisinflammation can be purely mechanical (e.g., stress; tension) orchemical (e.g., copper and/or zinc coating; inflammatory agent coating).As disclosed in further detail below, a chemical agent could also bedelivered to the target site by a local delivery mechanism (such as alocal drug delivery balloon) prior to or following device delivery. Thebody's response to the inflammation is to attack the inflammation,thereby producing excess interstitial fibrous tissue which preventsconduction or generation of irregular signals.

[0074] In addition to inducing fibrosis, the present invention may alsobe used to induce calcification of the adventitial region within avessel, such as the pulmonary vein 44. The calcification processfunctions to harden soft tissue which interrupts electrical conductionof atrial impulses and, thus, prevents AF impulses from spreading to theatrium. Further, calcification of the coronary sinus can also beperformed, in the event that the coronary sinus is involved in thearrhythmic circuit. In general, calcification may be induced inpractically any tissue region exhibiting arrhythmia.

[0075] One method of inducing calcification is to take blood directlyfrom a patient and inject it into the vascular wall. Alternatively, theblood may be concentrated, for example, by methods of centrifugation orsedimentation by gravity. Since the red blood cells are the apparentinducers of calcification, the blood is first concentrated to separateout these red blood cells. Next, a sufficient amount of red blood cellsare then injected directly into the wall of the vessel. Consequently,the tissue 36 becomes relatively hardened or inflexible due tocalcification, thereby suppressing or terminating irregular rhythmconduction.

[0076] The above-discussed injection may be accomplished using a localdrug delivery catheter such as the Infiltrator (manufactured byBoston-Scientific Corp.). The Infiltrator has small needles capable ofdelivering injectate through the needles and into the wall of thevessel. However, care should be taken so that the needle does notdissect the vessel wall during the injection process. As such, smalldissections may be more beneficial and induce a higher calcific volumecompared to larger dissections.

[0077] In an alternate embodiment of the invention, the device 30 mayalso be used to prevent or slow growth/expansion of aneurysms. Ingeneral, the device 30 creates fibrosis and collagen deposition andpromotes cellularity of the aneurysms to hemodynamically stabilize them,thereby preventing growth and rupture. This is accomplished by initiallygenerating a temporary inflammatory reaction that heals with a fibroticlayer. The resulting fibrosis contains cellularity, a feature thatsustains the fibrosis, attaches the device 30 to the artery wall, andprovides for long-term stabilization of the biologic-technologic hybridcombination.

[0078] This embodiment of the device 30 comprises a percutaneous implantthat expands, either through a self-expanding mechanism (similar tothose described previously and in further detail below) or via aballoon-expanding mechanism. The device 30 may further exhibit excellentlongitudinal and trans-axial flexibility, enabling it to optimallyconform to the vessel wall. As such, the device 30 provides a supportingstructure that effectively presses the device 30 against the wall of theaneurysm, preventing both expansion and rupture of the aneurysm. Thefibrosis serves to irreversibly attach the device to the vessel wall.

[0079] In general, a variety of device configurations may be used totreat, prevent and terminate aneurysms. For example, the device 30 maybe coated with a chemical (similar to those described previously and infurther detail below) that induces an inflammatory response. Inaddition, the device 30 may also include a large structural componentcombined with a fine netting or mesh. This configuration may provideimproved coverage of the internal surface of the aneurysm. As such, whenthe inflammatory material is pressed against or contacts the intima ofthe vessel, this induces a subsequent inflammatory response.Additionally, the material may be made to expand only to a certainpoint, and then become quite stiff/rigid, thereby limiting furtherexpansion of the device 30 and/or aneurysm.

[0080] In an alternate embodiment, the material structure orconfiguration of the device 30 alone may be sufficient to stimulate athickened response (e.g., cellularity) or create tension that makes theadventitia ischemic. These mechanisms may be similar to those by which astent induces fibrosis and neointimal thickening in a vessel. Thus, insome instances, the device 30 simply needs to be pressed against thewall of the vessel to induce the desired fibrotic response.Alternatively, it may be the intimal placement of the mesh/inflammatorycoating of the device 30 that generates the desired adventitialinflammatory response.

[0081] The above-described device 30 (and additional embodiments furtherdisclosed below) may be used to treat a variety of aneurysms, such asabdominal aortic aneurysms, cerebral aneurysms and all peripheralaneurysms of arterial or venous structures. For example, the device 30may be positioned in the abdominal aorta of a patient with a small tomoderate sized aneurysm. This device 30 may also be configured toprevent radial expansion both by mechanical features of the strut andalso by the fibrous structure of the induced tissue response. As aresult, the device 30 fibroses the aortic wall, gives it a cellularnature, thickens the wall, increases the structural integrity of theorgan/abdominal aorta at the aneurysm site, attaches to the wall and/orprevents expansion. The aneurysm is thus “frozen” in size and cannotcontinue to grow (i.e., limited device expansion also limits aneurysmexpansion). This result eliminates the need for future surgical repairand, further, is prophylactic for aneurysm growth.

[0082] Similar to the above-described abdominal aneurysm, cerebralaneurysms may also be treated using the device 30 of the presentinvention. The device 30, generally smaller in size, strengthens thestructural integrity of the organ at the aneurysm site and, thus,prevents both expansion and rupture due to the resulting thickened wallstructure (i.e., cellularity).

[0083] The device 30 of the present invention may be used in a varietyof additional applications. In one embodiment, the device 30 may beplaced in a vein graft (e.g., saphenous vein graft) that is beginning todegenerate. The device 30 functions to “reline” the vein graft with alayer of device material and/or tissue 36. In general, the density ofmaterial determines the amount of cellularity and neointima produced.

[0084] In an alternate embodiment, the device 30 may be placed in a veinto “shrink” the venous size, thereby restoring venous valve patency. Inyet another embodiment, the device 30 is positioned to encircle theentire atrium, thus providing full internal support as the fibroustissue develops and restoring/maintaining normal atrial contraction. Inanother embodiment, the device 30 may be positioned internally of theheart as one or more atrial rings. Fibrous tissue growth induced by thedevice 30 may not only prevent undesired atrial expansion but, further,may terminate AF. In an alternate embodiment, the internally implanteddevice 30 promotes formation of an endocardial encircling ring thatprevents ventricular infarct expansion and, in some instances,ventricular remodeling.

[0085] In another embodiment, the device 30 of the present invention maybe an elastic band, passive (i.e., requires no energy) andpercutaneously implantable device 30 that functions as an arterial shockabsorber when implanted at a target site. For example, when placed in anartery or other structure, the device 30 modifies the elasticity of thatstructure (i.e., the pressure-volume relationship of the structure in afixed manner that may be linear, or any other simple mathematicalfunction).

[0086] To better understand the mechanisms and functionalcharacteristics of this embodiment of the device 30, a general review ofblood flow and blood pressure and their affects on vessels/organs ishelpful.

[0087] In general, blood pressure and flow are in phase (i.e., the phaseangle between them is zero) when pulsatile flow is instituted in apurely resistive structure. However, blood flow within the humanvasculature is further complicated by curves, bifurcations and vesselcompliance. As such, the normal human aorta and large capacitancevessels are not purely resistive structures. The pressure-flowrelationship in these organs is partially capacitive, since the walls ofthese organs expand and contract with the pumping of blood. As a result,pressure and flow differ in phase and, in particular, flow typicallyleads pressure for pulsatile waveforms, such as those induced by a bolusof blood ejected by the heart into the aorta with each cardiac cycle.

[0088] As the human vessel ages it becomes significantly stiffer,resulting in a more purely resistive (less compliant) structure. Thismeans that the blood pressure rises simply because of the arterialstiffness. The heart must expend more work on each heartbeat to pump theblood throughout the body at the higher pressure. Arterial stiffness isa major cause of high blood pressure and, in the long turn, heartfailure if the hypertension is not treated. Literally millions of peopleare under treatment (typically with medication) for hypertension andheart failure.

[0089] The device 30 of the present invention, when elastic and placedin the aorta or great vessels, restores elasticity (as previouslydescribed and discussed in further detail below) to aging cardiovascularsystems that have become stiff, rigid, and cause hypertension. If theapplied pressure-volume relationship of the implantable device 30 isappropriately nonlinear, the device becomes a “blood pressureregulator.” As such, the device 30 allows any blood pressure up to apre-defined limit, but prevents higher blood pressures than that limitby expanding to accommodate the volume of ejected blood and preventpressure rises. By restoring a capacitive vector to the centralcirculation, the device 30 actually lowers blood pressure withoutpharmacology.

[0090] In general, the device 30 functions as a passive, hydraulicsystem that absorbs volume in proportion to pressure and has a rapidfrequency response. In one embodiment, the device 30 is configured as ascaffold (with, for example, a stent-like configuration) that grows intothe artery and becomes part of the vessel. In effect, the device 30functions as an “arterial shock absorber” after implant. The followingare several examples of various embodiments of the device 30 used totreat hypertension.

[0091] In one embodiment, shown in FIG. 5A, the stent-like device 30includes two concentric, tubular-shaped members 68, 70 that function asa shock-absorber to blood flow/pressure. For example, as a bolus ofblood is pumped out of the heart and into the target site where thedevice 30 is positioned, the inner member 68 of the device 30 compressesagainst the outer member 70, thereby absorbing, partially or totally,the volume of ejected blood to maintain normal pressure within thesystem. Generally, the amount of compression is proportional to thepressure; however, nonlinear compression-pressure relationships may alsobe desirable (as described above) to generate unique properties, such asblood pressure regulation. In some instances, the volume of fluid/bloodabsorbed may be up to 20% or more of the stroke volume.

[0092] In an alternate embodiment, the device 30 may be a fiber band ona circumferential support structure that stimulates elastin growth. Asshown in FIGS. 8C-8E, the device 30 may be partially or completelycovered with elastin or an elastin epitope. In this configuration, thedevice 30, in essence, functions to restore the capacitive vector to thevessel/organ 36. For example, as the heart ejects a bolus of blood into,for example, the aorta, the elastin expands to partially accept thevolume, thereby preventing the blood pressure from rising as high aswould be the case were the vessel rigid (i.e. without the device 30). Ingeneral, the amount of expansion is proportional to the pressure.

[0093] As discussed in further detail below, the device 30 may befabricated from a variety of materials and configured into variousdesigns. In one embodiment, the device 30 may be completely elastic, dueto its material and/or structural characteristics. Alternatively, thedevice 30 may be elastic and include pores that promote cellular ingrowth so that the device 30 becomes a living structure within the body.

[0094] By restoring the elastic pressure-volume capacitiverelationships, the device 30 is useful as a passive (e.g. non-powered),non-pharmacologic method for treating heart failure. This is true notonly because blood pressure is lowered, but also because the energy ofthe failing heart is more efficiently coupled to the arterial system viathe compliant nature of the device 30. Thus, if the device 30 functionswith minimal energy loss, then the energy is more efficiently coupled.

[0095] For example, in one embodiment of the invention, illustrated inFIG. 5B, one or more springs 72 (e.g., Nitinol® springs) are locatedbetween the two membranes 68, 70 of the device 30. The springs enablethe device 30 to function with minimal energy loss such that theresulting system actually conserves energy, an importantfeature/attribute for cases with failing hearts.

[0096] In an alternate embodiment (not shown), the biocompatible device30 includes inflammation inducing features (e.g., structural, chemical,etc.) either on the entire device 30 or on a portion of the device 30.The inflammation may further induce fibrosis which functions to “glue”the device 30 to the inside of an artery or other organ.

[0097] In yet another embodiment, the device 30 may also be configuredto function as a bladder-like system. This system may includecompressibility features that decrease volume with increasing bloodpressure.

[0098] Although generally passive, the device 30 may include certainfeatures or mechanisms that are externally programmable. Examples ofsuch features/mechanisms include, but are not limited to, variablecompliance, variable compressibility, and variable expandability. Forexample, referring to FIG. 5B, one or more Nitinol® springs of thedevice 30 may be heated externally in order to change the springconstant. Changing the spring constant may increase (or decrease,depending on the type of change) the amount of device compressibility tothat which is more proportional to the hypertension. The ability totranscutaneously heat Nitinol® may yield other programmable features,not disclosed herein but known to those skilled in the art, which arealso included within the scope of the claimed invention.

[0099] In another embodiment of the invention, the device 30 may includefeedback capabilities. For example, the device 30 of the presentinvention may measure and transmit pressure readings to anotherimplantable device, such as a biventricular pacing system. Thisconfiguration permits literal and real-time feedback to optimize energytransfer and heartbeat within the system.

[0100] As previously described, the device 30 is generally a passive,non-powered device. However, these communication or sensing features ofthe device 30 may require a source of power in order to properlyfunction. In one embodiment, this can be accomplished via thecompression/expansion capabilities of the device 30. As the bloodpressure causes the device 30 to compress/expand, this energy, in turn,can be captured to generate electrical energy which can then betransferred to power the system. Alternate energy generating systems andmeans, not disclosed herein but known to those skilled in the art, mayalso be used and are also included within the scope of the claimedinvention.

[0101] Referring to FIGS. 6A, 6B and 7, an alternate embodiment of theimplantable device 30 in accordance with the present invention includesat least one elongate element 32 and one or more protrusions or graspingmembers 34 that extend into or through tissue 36. In general, the device30 comprises a sterile biocompatible material and may be percutaneouslyor surgically implanted on either an endocardial or epicardial surfaceof the heart. In an alternate embodiment, the device 30 may be implantedwithin a lumen of the heart. The size and configuration of the device30, including the materials from which it is made, are tailored toproperly conform to tissue requirements and desired device-inducedresults. Although the invention as disclosed herein generally refers tothe heart, other body organs and cavities, such as pulmonary veins,coronary artery, coronary vein, renal artery, renal vein, aorta,cerebral vessels, coronary sinus or other similar cavities/organs, arealso included within the scope of the present invention.

[0102] As shown in FIG. 8A, an alternate embodiment of the device 30 ofthe present invention may include a plurality of elongate elements 32configured to form a mesh-shaped device 30. This device 30 configurationnot only increases the surface area of the device 30 that contactstissue 36, but may also enhance the structural integrity, flexibilityand tissue adhesion characteristics of the device 30.

[0103] In an alternate embodiment, shown in FIG. 8B, the elongateelements 32 may be rod-shaped to form a type of fiber. The fiber-shapedelement 32 may be used alone or in combination with other devices. Forexample, referring to FIG. 8C, the fiber-shaped element 32 may becombined with a fabric or net 38, thereby functioning as a structuralcomponent of the resulting device 30. During use, the device 30 producesthe desired fibrotic response through proper tissue contact, shown inFIG. 8D, and/or by becoming integrated within, the tissue 36, as shownin FIG. 8E. Additional details concerning device structure and tissueresponse are described in further detail below.

[0104] One or more of the elongate elements 32 or simply portions of theelongate elements 32 may also be configured to an increasedthickness/diameter, which may provide increased strength and structuralintegrity to the overall device 30. Additional device 30 configurationsincluding, but not limited to, ribbon-shaped, spherical, cubical,tubular, rod-shaped, net-shaped, ring-shaped, sheet-shaped and woven,including combinations thereof, are also within the scope of the claimedinvention.

[0105] The grasping members 34 of the present invention are generallydesigned to be pushed into and attached to tissue 36, such as muscle, asdescribed in further detail below. These grasping members 34 anchor thedevice 30 to the tissue 36 and, thus, prevent the device 30 fromslipping/dislodging or causing embolization within the patient. As such,the grasping members 34 may be configured as darts, studs, barbs,prongs, pointed structures, capped rods and other designs for secureattachment to and/or permanent placement within tissue 36.

[0106] A variety of methods may be used to urge the grasping members 34into the tissue 36. Examples of such methods include, but are notlimited to, a radially expanding balloon, a self-expanding device 30(due to material characteristics of the device 30 or structuralcharacteristics, such as internal struts), an expanding tool, ormechanical force by a physician.

[0107] Although the device 30 illustrated in FIGS. 6A-8E includes atleast one grasping member 34 designed to penetrate partially orcompletely through tissue 36, the device 30 may also be configured toinclude no grasping members 34. Tissue adhesion or attachment may beaccomplished via structural or chemical characteristics of the device30. For example, the device 30 may be configured to conform and,thereby, adhere to an internal or external area of a body cavity.Alternatively, the device 30 may be fabricated from porous materialsthat promote tissue adhesion and subsequent biological anchoring.Permanent cellular in-growth may further transform the device 30 into aliving structure. As such, the living nature of the device 30 permits itto become integrated and thereby last for long periods of time withinthe body.

[0108] Examples of porous materials used with the device 30 of thepresent invention include, but are not limited to, ceramics, alumina,silicon, Nitinol®, stainless steel, titanium, porous polymers, such aspolypropylene, ePTFE, silicone rubber, polyurethane, polyethylene,acetal, nylon, polyester, and any combination of such materials.Although these materials (and others not specifically described, butincluded in the scope of the claimed invention) may not be inherentlyporous, various manufacturing and processing techniques may be used togive the materials the desired porosity characteristics.

[0109] In one embodiment of the invention, the device 30 is made of aconductive material, such as stainless steel. Alternative biocompatiblematerials including, but not limited to, metals, ceramics, plastics,bioabsorbable materials, bioresorbable materials, biostable materials,absorbable materials, non-absorbable materials or biomaterials, eitheralone or in various combinations, may also be used.

[0110] In general, the device 30 of the present invention is used totreat, prevent and/or terminate arrhythmias. In one embodiment of theinvention, the device 30 is made of a conductive material, such as ametal, and functions as a voltage clamp to short circuit an arrhythmia.During use, the grasping members 34 of the device 30 are pushed into thetarget cardiac tissue 36. A single device 30 or multiple devices 30 maybe placed over a portion or circumferentially around a cardiac chamber,such as the atrium or ventricle, depending on the type and location ofthe arrhythmia. For example, in the case of multiple devices 30, thedevices 30 may be placed in parallel (i.e., multiple equatorial bands,shown in FIGS. 9A and 9B) or combined to form equatorial and polarrings, shown in FIGS. 10A and 10B, respectively.

[0111] After the grasping members 34 are inserted into tissue 36, themetallic properties of the device 30, particularly the grasping members34 which are also made of metal, cause the device 30 to hold theintramyocardial tissue 36 at the same isoelectric potential across theentire device 30. Additionally, when the grasping members 34 of thedevice 30 extend through the cardiac tissue 36, the isoelectricpotential also extends through the entire transmural muscle. As such,since all device-contacted muscle must be isoelectric, the device 30short-circuits the arrhythmia. Examples of arrhythmias that may beshort-circuited by the device 30 include, but are not limited to, atrialfibrillation, reentrant supraventricular tachycardia (SVT), ventriculartachycardia (VT) and Junctional Tachycardia.

[0112] In an alternate embodiment, the device 30 of the presentinvention may also be used to isolate localized sources of arrhythmias.As previously discussed in the Background of the Invention, somearrhythmias may be triggered or maintained by a single focus ofautomatic firing. To prevent the aberrant signal from propagatingthroughout the cardiac muscle, the elongate member 32 is configured intoa generally ring-shaped device 30, as illustrated in FIG. 11. However,it is understood that other device configurations optimized to isolatethe particular arrhythmia at a specific tissue site may also be used andare hereby included within the scope of the claimed invention.

[0113] The device 30 is then positioned to contact the tissue 36 andsurround that portion of muscle from which the arrhythmia originates.For example, the device 30 may be located on a portion of either anendocardial 40 or epicardial 42 surface of an atrium, ventricle orvessel (such as a pulmonary vein), shown in FIGS. 12A, 12B, 12C and 12D.Alternatively, as illustrated in FIGS. 12E, 12F and 12G, the device 30may be positioned to surround one or more of the pulmonary veins 44 oneither an endocardial 40 or epicardial 42 surface of the heart. Asanother example, the device 30 may be placed on an internal surface oran external surface of a pulmonary vein 44. The metallic nature of thedevice 30 together with its tissue-contacting characteristics create ablock thereby preventing conduction of the impulse beyond the confinesof the device 30 and, ultimately, short-circuiting the arrhythmia.

[0114] In another embodiment of the invention, one or more biologics,drugs or other chemicals/agents may also be included with the device 30.The chemical may be bound, for example, to at least a portion of thesurface and/or interior of the elongate members 32 and/or graspingmembers 34 of the device 30. For example, the grasping members 32 may behollow allowing the chemical to elute from the hollow area of thegrasping members 34 and into the tissue 36. Alternatively, if the device30 is fabricated from porous materials (as discussed above), thechemical may be contained within and released from the pores and intothe tissue 36.

[0115] During use, the chemical/agent is released into the myocardialtissue 36 or simply interfaces with the tissue 36 as it contacts thedevice 30. In an alternate embodiment, the chemical, which may be acoating that is bioabsorbable (or biostable), dissolves or erodes anddisappears over time. In yet another embodiment, the chemical promotesformation of an endothelial lining and, eventually, a neointimal layer,thereby encasing the device within the tissue. Alternatively, thechemical may be an anti-thrombotic material that functions to preventclot formation and/or embolization from the implanted device 30.

[0116] As a result, the chemical may depress or prevent conduction ofaberrant impulses, affect the electrophysiology of the heart to maintainnormal sinus rhythm, act as a therapeutic agent, terminate arrhythmiasor induce other desired tissue and system responses. Examples of thesechemicals/agents include, but are not limited to, blood, copper, zinc,nickel, polylactic acid, polyglycolic acid, heparin, plateletglycoprotein IIb/IIa inhibiting agent, tetracycline, lidocaine, starch,paclitaxel, adriamycin, alcohol, fibrosis inducing agents, inflammatoryinducing agents, anticoagulants, polymers, drug-eluting polymers,macrophage chemoattractant protein, chemoattractants, therapeutic drugsand other agents/chemicals.

[0117] In addition to providing an effective means of treatingarrhythmias, the device 30 and methods of use of the present inventioneffectively reduce pain, infections and postoperative hospital stays.Further, the various treatment methods also improve the quality of lifefor patients.

[0118] Although the invention has been described in terms of particularembodiments and applications, one of ordinary skill in the art, in lightof this teaching, can generate additional embodiments and modificationswithout departing from the spirit of or exceeding the scope of theclaimed invention. Accordingly, it is to be understood that the drawingsand descriptions herein are proffered by way of example to facilitatecomprehension of the invention and should not be construed to limit thescope thereof.

What is claimed is:
 1. A method of treating cardiac arrhythmiascomprising: delivering a treatment device to a target site; manipulatingsaid device to conform a shape of said device to a shape of said targetsite; modifying a tissue makeup at the target site; allowing saidmodification of tissue makeup to proceed so as to induce a response thatresults in electrically decoupling said tissue; and leaving saidtreatment device implanted at said target site.
 2. A method as set forthin claim 1, wherein delivering a treatment device to a target siteincludes delivering said device to a body cavity.
 3. A method as setforth in claim 2, wherein delivering a treatment device to a target siteincludes delivering said device to a pulmonary vein.
 4. A method as setforth in claim 3, wherein delivering a treatment device to a target siteincludes delivering a stent to said pulmonary vein.
 5. A method as setforth in claim 2, wherein delivering a treatment device to a target siteincludes delivering said device to an ostium of a pulmonary vein.
 6. Amethod as set forth in claim 5, wherein delivering a treatment device toa target site includes delivering a stent to said ostium of saidpulmonary vein.
 7. A method as set forth in claim 6, whereinmanipulating said device further conforms said target site to said shapeof said device, bringing said ostium into a lumen of said device.
 8. Amethod as set forth in claim 2, wherein delivering a treatment device toa target site includes delivering said device to a left atrium.
 9. Amethod as set forth in claim 8, wherein delivering a treatment device toa target site includes delivering a stent to said left atrium.
 10. Amethod as set forth in claim 1, wherein modifying the tissue makeup isperformed by stretching said tissue.
 11. A method as set forth in claim10, wherein stretching said tissue does not produce tissue laceration.12. A method as set forth in claim 10, wherein stretching said tissueinduces tissue laceration.
 13. A method as set forth in claim 10,wherein stretching said tissue induces organ ischemia.
 14. A method asset forth in claim 10 wherein stretching said tissue induces fibrosis.15. A method as set forth in claim 1, wherein modifying the tissuemakeup includes mechanically impairing at least a portion of saidtissue.
 16. A method as set forth in claim 15, wherein mechanicallyimpairing said tissue includes penetrating said tissue with pointedstructures fixed on said treatment device.
 17. A method as set forth inclaim 1, wherein modifying the tissue makeup includes mechanicallychanging at least a portion of said tissue.
 18. A method as set forth inclaim 17, wherein mechanically changing at least a portion of saidtissue includes distorting a geometry of an ostium such that atrialcells at an ostial site are repositioned within a lumen of said device.19. A method as set forth in claim 1, wherein disrupting the tissuemake-up includes introducing a bioactive agent to said target site. 20.A method as set forth in claim 19, wherein said bioactive agentcomprises a metallic coating.
 21. A method as set forth in claim 1,wherein more than one treatment device is delivered to more than onetarget site.
 22. A method as set forth in claim 21, wherein said targetsite is selected from the group consisting of right pulmonary venousostium, left pulmonary venous ostium, right pulmonary arterial ostium,left pulmonary arterial ostium, right pulmonary vein, left pulmonaryvein, right pulmonary artery, left pulmonary artery, coronary sinus,atrial tissue and any combination thereof.
 23. A method as set forth inclaim 1, wherein modifying said tissue makeup at the target siteincludes inducing inflammation.
 24. A method as set forth in claim 1,wherein modifying said tissue makeup at the target site includesinducing fibrosis.
 25. A method as set forth in claim 1, whereinmodifying said tissue makeup at the target site includes inducingelastance caused by elastin synthesis.
 26. A method as set forth inclaim 1, wherein modifying said tissue makeup at the target siteincludes inducing calcification of said tissue.
 27. A method as setforth in claim 1, wherein modifying said tissue makeup at the targetsite includes inducing cell proliferation.
 28. A method as set forth inclaim 1, wherein modifying said tissue makeup at the target siteincludes inducing collagen formation.
 29. A method as set forth in claim1, wherein modifying said tissue makeup at the target site includesinducing extra-cellular changes.
 30. A method as set forth in claim 1,wherein modifying said tissue makeup at the target site includesintroducing a therapeutic drug.
 31. A device for modifying conduction,electrical connection and propagation properties in a tissue comprising:a structural platform made of a biocompatible material; said platformconformable to a shape of a target tissue site; said platform having atreatment component sized and shaped to induce a fibrotic response insaid target tissue; and, said treatment component being configured tocause sufficient fibrotic response so as to substantially eliminate saidcardiac arrhythmias.
 32. A device according to claim 31, wherein saidplatform presses against said target tissue to leave at most a minimalgap.
 33. A device according to claim 31, wherein said structuralplatform is an implantable pulmonary vein support structure.
 34. Adevice according to claim 33, wherein said treatment component includespointed structures fixed on an external surface of said pulmonary veinsupport structure.
 35. A device according to claim 33, wherein saidstructural platform is a pulmonary vein stent.
 36. A device according toclaim 33, wherein said structural platform is a coronary sinus stent.37. A device according to claim 33, wherein said structural platform isa cardiac vein stent.
 38. A device according to claim 33, wherein saidstructural platform is an arterial tissue stent.
 39. A device accordingto claim 33, wherein said structural platform is a pulmonary arterystent.
 40. A device according to claim 31, wherein said structuralplatform is an implantable coronary sinus support structure.
 41. Adevice according to claim 31, wherein said structural platform is animplantable cardiac vein support structure.
 42. A device according toclaim 31, wherein said structural platform is an implantable arterialtissue support structure.
 43. A device according to claim 31, whereinsaid structural platform is an implantable pulmonary artery supportstructure.
 44. A device according to claim 31, wherein said structuralplatform is conformable to substantially an internal shape of apulmonary vein.
 45. A device according to claim 31, wherein saidtreatment component includes a therapeutic substance.
 46. A deviceaccording to claim 45, wherein said treatment component includes aplurality of pointed structures.
 47. A device for modifying tissue at atarget tissue site of an organ comprising: at least one deploymentplatform; said deployment platform including a treatment componentconfigured to induce a material tissue response at said target tissuesite; and said treatment component configured to induce a materialtissue response sufficient to modify local physiologic properties ofsaid organ so as to achieve a desired therapeutic goal for said organ.48. A device according to claim 47, wherein said organ includes a heartand associated cardiopulmonary vessels.
 49. A device according to claim48, wherein said tissue site includes tissue associated with a pulmonaryvein.
 50. A device according to claim 49, wherein said tissue includestissue comprising a pulmonary ostium.
 51. A device according to claim48, wherein said therapeutic goal is the electrical decoupling of saidtarget tissue.
 52. A device according to claim 47, wherein said organincludes an abdominal aorta.
 53. A device according to claim 52, whereinsaid therapeutic goal comprises an increase in structural integrity ofsaid organ at an aneurysm site.
 54. A device according to claim 53,wherein said material tissue response is a fibrotic response.
 55. Adevice according to claim 52, wherein said therapeutic goal is toincrease elasticity of said tissue at said target tissue site.
 56. Adevice according to claim 47, wherein said deployment platform is a bodylumen support structure.
 57. A device according to claim 56, whereinsaid body lumen support structure is a stent like structure.
 58. Adevice according to claim 48, wherein said body lumen support structureis sized and shaped for placement into a pulmonary vein.
 59. A deviceaccording to claim 47, wherein said body lumen support structure issized and shaped for placement in an abdominal aorta.
 60. A deviceaccording to claim 47, wherein said deployment platform is sized andshaped for placement on an external surface of a body organ.
 61. Adevice according to claim 60, wherein said deployment platform is sizedand shaped for placement on an external surface of a pulmonary vein. 62.A device according to claim 57, wherein said treatment componentincludes mechanical barbs.
 63. A device according to claim 57, whereinsaid treatment component includes a chemical coating on said stent-likestructure.
 64. A method of inducing a material tissue response at atarget site comprising: delivering a treatment device to said targetsite; ensuring contact of a treatment component of said treatment devicewith tissue at said target site; inducing said material tissue responseat said target site as a result of ensuring contact of said treatmentcomponent with said tissue; allowing said material tissue response tocontinue at said target site at least until a therapeutic goal issubstantially achieved.
 65. A method according to claim 64, wherein atherapeutic goal of electrical decoupling of said tissue is achieved.66. A method according to claim 65, wherein an electrical decouplingresulting in the elimination of cardiac arrhythmias is achieved.
 67. Amethod according to claim 66, wherein delivering a treatment device to atarget site includes delivery to a region that at least includes apulmonary ostium.
 68. A method according to claim 67, wherein deliveringsaid treatment device includes delivery to a region that furtherincludes a pulmonary vein.
 69. A method according to claim 64, whereininducing the material tissue response includes inducing fibrosis.
 70. Amethod according to claim 64, wherein inducing the material tissueresponse includes inducing elastance.
 71. A method according to claim64, wherein a therapeutic goal of increasing structural integrity ofsaid tissue is achieved.
 72. A method according to claim 71, whereinincreasing structural integrity includes reinforcing tissue of anabdominal aorta in a region of an aneurysm.
 73. A method according toclaim 64, wherein ensuring contact of a treatment component with saidtissue includes ensuring contact of a drug with said tissue.
 74. Amethod according to claim 64, wherein ensuring contact of a treatmentcomponent includes urging mechanical barbs of said treatment device intosaid tissue.